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SGU Physiology - ANS Pharmacology
SGU Physiology ANS Pharmacology drugs.
Terms in this set (42)
Distinguishing pharmacologic characteristics:
Blocks release of Ach from cholinergic nerve terminals by cleaving SNAP-25 (a protein required for release of synaptic vesicles)
Excessive muscle paralysis
Principal clinical uses:
Mode of Action: Inhibits synthesis of Ach by competing with choline for transport into the cholinergic nerve terminal.
No clinical applications and will not be discussed further.
Anticholinesterases - Method of action
indirectly acting parasympathomimetic agents. Normal dose improves transmission at cholingergic synapses. Very high does result in poisoning (SLUD- salivation, lacrimation, urination, and defecation). Prototype is neostigmine. Prototype insectidice is DFP. Contraindications: asthmatics, hyperthyroid (susceptible to arrhythmias), peptic ulcer, or intestinal/bladder obstruction.
Anticholinesterases - Uses
1. Improve transmission at the NMJ
a. Myasthenia gravis
b. Lambert-eaton disorder
2. Increase PS tone
a. Glaucoma - miosis increases outflow of aq.
humor, reducing IO pressure
b. Relieve abdominal distension - increase gut mobility (SE: salivation, acid secretion)
c. To treat atropine poisoning
3. Increase cholinergic activity in the CNS
a. Alzheimer's Disease - helps improve cholinergic transmission
Anticholinesterases - List
a.k.a. Tensilon: reversible AchE Inhibitor; Short-acting indirect muscarinic agonist; Dx of myasthenia gravis
reversible anti-ChE. Tertiary so it can cross the BBB (important feature). Duration 1-2 hours. Oral or parenteral admin. Used to treat glaucoma. Antidote for atropine overdose. ("Phyxes" the atropine overdose)
reversible anticholinesterase; treats post-op and neurogenic ileus and urinary retention, myasthenia gravis, reversal of neuromuscular junction blockade; doesn't cross BBB
Irreversible anticholinesterase. Excessive stimulation of nicotinic receptors - muscle weakness and paralysis. Excessive parasympathomimetic effects - salivation, bronchoconstriction, miosis, bradycardia, increased GIT motility and tone. The potentially fatal adverse effect is paralysis of the respiratory muscles. Posioning by this drug can be treated with pralidoxime or atropine.
(2-PAM) Supplements atropine in therapy for O-P intoxication. Acetylchoinesterase reactivator by releasing phosphoryl moiety to restore AChE activity. Must be given before "aging" occurs. Can restore NMJ in minutes.
plant alkaloid from Atropa belladonna, It binds to muscarinic receptors and prevents Ach from exerting its effects. prototype muscarinic antagonist found in jimsonweed and has significant clinical utility. Tertiary amine-crosses BBB. Depresses PNS activation: pupillary dilation, cycloplegia (ciliary m), bronchiolar dilation, constipation, urine retention, decreased secretion, AND decreased sweating (SNS). Drug of choice to treat spasms of GI tract. Therapeutic uses: dilate pupil and cycloplegic for eye exam, COPD/asthma, colic, bed-wetting, peptic ulcer, adjunct to neostigmine for intubation, increase HR during anesthesia, antidote for anti-ChE poisoning, Parkinsons. Overdose is toxic.
nicotinic antagonist - skeletal muscle relaxants - depolarizing - has some efficacy - short acting - not broken by ACHe - metabolized by BuChE - no reversal - will antagonize tubocurarine, depolarizing antagonist, fast onset, short acting, release of histamine, no ganglionic blockade - depends on dose, hydrolyzed by pseudocholinesterase, release of potassium --> can result in arrythmias, CV reactions depend on ganglionic stimulation, can either see decreased HR and BP (from cardiac muscarinic stimulation and increase in EDRF) or increased bp (MOST of the time - sympathetic response)
muscarinic agonist: a direct parasympathomimetic. A tertiary amine with SAR for MAChR. Not hydrolyzed by ChEs. A 3rd line drug in the treatment of glaucoma- admin as eyedrops. Contracts circular muscle of pupil to widen angle, improves trabecular tone. plant alkaloid
muscarinic agonist; treats glaucoma by contracting pupils and realeasing intraocular pressure, semisynthetic derivative of Ach
Ganglionic NN rec antagonist, nicotinic antagonist; ganglionic blocker. used in experimental models to prevent vagal reflex responses to changes in blood pressure- prevents reflex bradycardia caused by NE. Toxicity- severe orthostatic hypotension, blurred vision, constipation, sexual dysfunction;
Neuromuscular Nm antagonist. Oldest nondepolarizing nuromuscular blocking agent. Competes with ACh for binding to nicotinic M receptors. Paralytic agent and general anest. Drops BP does not cross BBB. Does NOT decrease consciousness.
Muscarinic Antagonist. Used as a patch. Affects the CNS and used in Motion sickness and anti-nausea end of life care.
Muscarinic antagonist. GI, used for Peptic ulcer.
Muscarinic Antagonist affecting respiratory tract. Used in COPD, Asthma. I PRAY I can breathe soon!
VMAT-2 blocker. Blocks active transport of amines into vesicles. Transient massive efflux of catecholamines followed by depletion of NE, DA, serotonin. Used in hypertension treatment, but has severe side effects (suicidal depression, hypotension, movement disorders)
Increases NE release from terminal. If ingested with MAOI's, this can cause a hypertensive crisis. Found in wine and cheese.
Indirect sympathomimeticPotent CNS stimulation via increased levels of NE due to:1) NE displacement from vessicles2) competitive inhibition of NE reuptake3) Inhibits MAO in presynaptic terminalCrosses BBB (not a catechol)Effects: increase energy, decrease fatigue, decrease appetite, decrease sleepToleranceSide effects: psychotic conditions, arrhythmias, dissecting aneurysms, hypertensionMethamphetamine more potentMethylphenidate (ritalin) used in ADHDModafinil- alpha and beta-1 activity used in narcolepsy
Alkaloid from Ephedra plant, Acts directly as adrenergic agonist on alpha and beta receptors, Acts indirectly by releasing NE, Has similar pharmacological effects as E, Stimulates the CNS (crosses BBB), Has a slower onset and longer DOA than E, Use topically: as a nasal and eye decongestant and a mydriatic, Systemically to increase blood pressure, As a bronchodilator; Continuous use causes tachyphylaxia
RITALIN: Noncompetitive NE & DA agonist (treat ADHD, improve attention)
potent NET inhibitor
Cocaine was used initially as a local anesthetic agent but its CNS effects were soon exploited! It is now classed as a drug of with a high abuse potential. Its CNS effects are similar to the amphetamines.
Tricyclic antidepressant (TCA), inhibit the NE transporter to prevent reuptake into the presynaptic neuron, adverse effects: sedation, confusion, incoordination
Monoamine oxidase inhibitor (MAOI): By blocking the metabolism of NE in the nerve terminals, MAOIs increase NE levels which provide more NE available for release into the synaptic cleft. Strongest treatment for TB infection. Tyramine ingestion is contraindicated.
Acts mainly as an alpha 1 selective agonist at therapeutic doses, Used topically as a decongestant for nasal and eye congestion, as a mydriatic (without cycloplegia), and for open-angle glaucoma (drug of choice), Used parenterally to increase blood pressure and treat paroxysmal supraventricular tachycardia, Chronic use can cause rebound nasal congestion
A1 agonist (IP3) used for SMC constriction for nasal or ocular decongestant. Sometimes as acute rescue for hypertension. SUDAFED
a2 agonist selective. T; hypertension, migraine, headache & hot flushes of menapause, ease of withdrawl symptoms of opiates, benzos, alcohol, nictine. side effect; sudden withdrawl leads to life threatening hypertensive crisis. inhibits release of catecholamines, decreases sympathetic outflow.
α2 agonist; Stimulates post-synaptic α2a receptors in CNS to block NE release; SE: Positive Coombs test, Na & fluid retention, hepatotoxic, fever, allergic skin reaction, hemolytic anemia, orthostatic hypotension (=XBBB)
Non-selective β agonist, adrenergic agonist. Beta non selective, ie b1=b2. Used to stimulate beta 2 adrenoceptors and relax bronchial smooth muscle. Used for A-V block and asthma.
Selective β1 agonist
Uses: acute management of heart failure (i.e. in an emergency situation)
(Note that β1 agonists are not generally used for the treatment of chronic heart failure because, although they increase force of contraction, they also increase the HR thus making the failing heart work harder.)
Selective β2 agonists:
Albuterol ("salbutamol" in the UK)
Salmeterol - has a long duration of action
The major uses of these drugs is in the relief of bronchoconstriction associated with asthma. They are powerful bronchodilators. The drugs can be administered by aerosolizing inhalers which deliver the drug to the site of action, thus minimizing adverse effects. (Some cardiac stimulation may occur, particularly after oral administration since the drug may have some slight activity on β1 receptors). The other side effect of these β2 agonists is due to their action on skeletal muscle which results in a slight tremor.
Non-selective, irreversible alpha blocker. Used in Pheochromocytoma before removing the tumor since high levels of released catecholamines will not be able to overcome the blockage.given with a beta blocker to treat pheo - beta must be given second or alpha will be unopposed and raise the bp super freaking high! Toxicity is Orthostatic Hypotension and reflex tachycardia.
Reversible Alpha blocker. Hypertension caused by pheochromocytoma. Causes postural hypotension. Phen=pheochromocytoma
adrenergic antagonist. Alpha 1 selective. Competitive antagonist. Epinephrine reversal and hypertension treatment. Action about 12 hrs, orally effective with little/no tachycardia due to a1 selectivity. Adjunct therapy for hypertension and used for urinary symptom relief (BPH).
a1blocker in prostrate. T; benign prostatic hyperplasia
Non-Selective β Antagonist "Beta Blocker"
Propranolol blocks the effects of the sympathetic nervous system on the heart resulting in decreased heart rate and decreased force of contraction. It leads to a reduction in blood pressure in hypertensive individuals but not in normotensives. Prolonged use leads to a fall in vascular resistance but the mechanism of this is not clear. Beta blockers also reduce the oxygen consumption of the heart. For this reason, they are given to patients suffering from angina.
Tx: Hypertension, Angina, Cardiac Arrhythmias, chronic cardiac failure, Essential tremor
adrenergic antagonist. Beta 1 selective. Antihypertensive. Medium action (6-9hrs). Few CNS effects, does not readily cross BBB.
nonselective beta blockerPartial agonist (ISA): means less change in cardiac output and heart rate (less loss of exercise tolerance)ISA- inhibits endogenous response in high levels of neurotransmitter, but creates a response in low levels of endogenous neurotransmitter
Used for trt of congestive hrt failure; contains 2 isomers, one with nonselective beta-blocker activity, and one with alpha-1 blocking activity
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